The findings indicated that the inflammatory response observed in MIS-C was distinct from the cytokine storm seen in severe acute COVID-19. Instead, it was similar to Kawasaki disease. However, there were differences, particularly concerning T cell subsets, interleukin (IL)-17A, and biomarkers associated with arterial damage. Furthermore, based on autoantibody profiling, it appeared that multiple autoantibodies might play a role in the development of MIS-C. Here, IL17A is linked to COVID-19.